Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3786_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
05.09.2026
Размер:
18 Мб
Скачать
332
https://t.me/med1917
Fig. 23.4 Bilateral lower
extremity lymphedema in a 56-year-old man before and after complex decongestive therapy. ( a ) Before treat- ment. Note the signifi cant limb swelling and chronic skin changes (lichenifi cation, warty projections, and cobblestone appearance) associated with lymphedema. ( b ) After treatment. Note the signifi cant improvement in limb swelling and chronic skin changes
J. Laredo and B.B. Lee
a
b
lymphedema with a female to male ratio of 10:1. It is usually unilateral and often limited to the foot and calf in most patients (Fig. 23.3 ) [ 2 , 8 , 11 ].
23.6 Secondary Lymphedema
Secondary lymphedema is far more common than primary lymphedema and represents 90 % of cases of lymphedema. The most common causes of lower extremity lymphedema are tumor (e.g., lymphoma, prostate cancer, ovarian cancer), surgery involving the lymphatics, radiation therapy, obesity, trauma, and infection. Worldwide, infection with the
parasitic nematode Wuchereria bancrofti (also known as fi lariasis) is the most common cause of lymphedema (Fig. 23.3 ) [ 2 , 4 , 8 ].
23.7 Diagnosis
23.7.1 Clinical Evaluation
Evaluation of patients with lymphedema must include a detailed, careful history and thorough physical examination [ 3 , 4 , 7 , 11 , 12 ]. The his- tory should include age at onset, travel to tropical countries, and history of all causes that could
23 Lymphedema
https://t.me/med1917
Fig. 23.5 Clinical signs of
lymphedema. ( a ) Positive Stemmer’s sign (a failure by the examiner to pick up or pinch a fold of skin at the base of the second toe). ( b ) Buffalo hump on the dorsum of the left foot in a patient with lymphedema
333
a
b
result in secondary lymphedema such as surgery, malignancy, venous insuffi ciency, trauma, and cellulitis. A history of temporary edema of the affected limb or other areas must be noted, and a detailed family history of limb swelling should also be recorded.
Signs and symptoms of lymphedema should be documented. These include nonpitting edema, skin changes such as “peau d’orange,”
pinkish- red skin discoloration, hyperkerato­sis, dermatitis, eczema, ulceration, varicosity, lymph vesicles, warty projections, drainage of fl uid (clear or milky), or yellow discoloration or other abnormalities of the nails (Fig. 23.4 ). The presence of Stemmer’s sign (inability to pinch a fold of skin at the base of the second toe) or puffi ness of the forefoot (buffalo hump) should be noted (Fig. 23.5 ) [ 3 , 7 , 11 , 12 ]. The
334
https://t.me/med1917
J. Laredo and B.B. Lee
presence of venous, arteriovenous, or capillary malformations and any limb length discrepancy should be recorded. Finally, any complications such as cellulitis, lymphangitis, malnutrition, and immunodefi ciency or, rarely, suspicion for malignancies (lymphangiosarcoma) must be documented [ 3 , 7 , 11 ].
23.7.2 Noninvasive Radiologic
Studies
Plain fi lm X-rays will identify limb length dis­crepancies, bone abnormalities, or phleboliths in patients with combined lymphatic malformations and venous malformations [ 7 , 11 ].
Venous duplex studies will confi rm any asso­ciated venous anomalies (valvular incompetence, obstruction, ectasia, or aneurysms) and assess for venous obstruction as an etiology or contributing factor to lymphedema [ 7 , 11 ].
23.7.3 Minimally Invasive Radiologic
Studies
Radionuclide Lymphoscintigraphy
This study is performed with a subcutaneous injection of 99mTc-labeled human serum albu­min (HAS) or 99mTc-labeled sulfur colloid (SC) into the fi rst and second web space of the toes (fi ngers), followed by radionuclide scanning at various time intervals [ 7 , 11 ]. It is the test of choice to confi rm or exclude lymphedema as the cause of chronic limb swelling. Removal of the colloid from the injection site; appearance time of activity at the knee, groins, or axilla; absence or presence of major lymphatic collectors; num­ber and size of vessels and nodes; the presence of collaterals and refl ux; and symmetric activity with the opposite side are recorded and used for interpretation.
An appropriate combination of non- to mini­mally invasive tests normally should provide all the information necessary to insure an adequate diagnosis and lead to the correct multidis­ciplinary, specifi cally targeted and sequenced treatment strategy. The tests and the information they provide are indicated here [ 11 ].
Basic/essential tests: Radionuclide lymphoscintigraphy MRI with/without contrast for the differential
diagnosis CT scan to exclude underlying pathology Duplex ultrasonography
Optional tests: Whole body blood pool scintigraphy (WBBPS) Magnetic resonance (MR) and/or ultrasound
lymphography Volumetry Bio-impedance spectrometry Air plethysmography Ultrasonographic lymphangiography: investiga-
tional for the reconstructive surgery candidate
patient MR lymphangiography: investigational for the
reconstructive surgery candidate patient Microscopic fl uorescent lymphangiography:
investigational for phlebolymphedema
Radionuclide lymphoscintigraphy is the most essential part of the diagnosis of lymph­edema in addition to clinical evaluation. This study is extremely useful for delineating the specifi c lymphatic abnormality and has largely replaced conventional oil contrast lymphog­raphy for visualizing the lymphatic network. Lymphoscintigraphy remains the gold standard for the lymphatic function evaluation, which is recommended for proper clinical management [ 3 , 7 , 11 ].
On some occasions an invasive study is required for an accurate diagnosis. These tests and the information they provide are listed below: Direct puncture percutaneous lymphangiography Standard (ascending) lymphangiography Indirect lymphography using water-soluble con-
trast media Fine needle aspiration biopsy of lymph node Skin biopsy in cases of suspected sarcoma and
skin cancer or differential diagnosis of warty
lesions
Invasive tests are seldom required for diagno­sis but are occasionally needed for confi rming the diagnosis or planning surgical therapy.
Conventional oil contrast lymphangiography, especially if coupled with computed tomography (CT) scanning, is still advantageous in selected patients with chylous dysplasia and gravitational
23 Lymphedema
https://t.me/med1917
335
refl ux disorders in order to defi ne more clearly the extension of the pathologic alterations and sites of lymphatic and chylous leakage [ 11 ]. It is the only diagnostic study that can clearly demon­strate pathologies of chylous vessels, chylous cyst, and thoracic duct in cases of chylothorax, chylous ascites, protein-losing enteropathy, etc.
As a part of the diagnostic procedure, the systemic causes of edema (e.g., heart failure, hypoproteinemia, pulmonary hypertension, hypo­thyroidism, cyclic edema) should be ruled out. Duplex ultrasonography should be performed initially in all forms of lymphedema to assess for concomitant venous disease.
Diagnostic evaluation should also include appropriate assessment of the patient’s under­standing of the disease process and ability to be compliant with the treatment regimen, since the outcome of successful management is totally dependent on the patient’s active participation in the care of his or her lymphedema.
23.8 Treatment of Lymphedema
23.8.1 General Considerations
The importance of patient education and compli­ance cannot be overemphasized when treating patients with both primary and secondary lymph­edema. The patient must fi rst understand that lymphedema is a chronic condition and will never be completely cured. In addition they must also understand that there is no “quick fi x” opera­tion, medication, or therapy that will completely reverse the clinical condition. Treatment of lymphedema is essentially management of the medical condition and prevention of progression of the disease process. Lymphedema can be suc­cessfully managed.
The goals of lymphedema therapy are to arrest progression, reduce swelling, maintain that reduction, prevent infection, restore mobility and range of motion, and train patients for self­management [ 4 , 10 , 14 ].
The treatment of lymphedema requires dili­gence and motivation on the part of the patient. The patient must be an active, compliant partici­pant for successful management. The mainstay of
lymphedema treatment is through physical thera­peutic measures occurring in the setting of a spe­cifi c lymphedema therapy program, performed by specially trained lymphedema therapists [ 3 , 10 , 14 , 15 ].
23.8.2 Physical Treatments
Physical treatment to reduce swelling is aimed at controlling lymph formation and improving lymph drainage through existing lymphatic ves­sels and collateral routes by applying normal physical processes which stimulate lymph fl ow (Table 23.2 ) [ 3 , 10 , 12 , 1416 ]. Manual therapies in multiple forms remain the most widely used interventions for the therapeutic management of lymphedema, regardless of etiology.
Table 23.2 Physical treatments for lymphedema
Treatment Effect Exercise Dynamic muscle contractions
encourage movement of lymph along tissue planes and noncontractile, initial lymph vessels (passive drainage) and increased contractility of collecting lymph vessels (active drainage)
Compression garments
Manual lymphatic drainage
Compression bandaging
Pneumatic compression
Elevation Does not stimulate lymph
Opposes capillary fi ltration Acts as a counterforce to muscle
contractions generating greater interstitial pressure changes
Form of massage therapy that stimulates lymph fl ow in more proximal, normally draining lymphatics to “siphon” lymph from congested areas
Used as an intensive treatment in combination with exercise to reduce large, misshapen lower limbs and permit subsequent maintenance treatment with compression stockings
Softens and reduces limb volume but can forcibly displace fl uid into the trunk and genitalia. Compression garments must be worn after treatment
drainage, but lowers venous pressure and therefore capillary fi ltration, allowing lymph drainage to catch up
336
https://t.me/med1917
J. Laredo and B.B. Lee
Table 23.3 Complex decongestive therapy
Phase I: intensive reduction therapy Manual lymphatic drainage massage Multilayered low-stretch wrapping techniques Specifi c exercise regimen Skin care education and techniques Phase II: maintenance therapy Daily wear of pressure garment Continued nightly multilayered wrapping Self-manual lymphatic drainage massage Exercise Continued meticulous skin management
Manual lymphatic drainage (MLD) is a highly specialized form of massage therapy that employs very light and gentle cutaneous distension to enhance lymph transport. MLD is believed to stimulate and increase the intrinsic contractility of lymph collecting vessels and encourage increased protein molecule sequestration and subsequent transport [ 10 , 1416 ]. MLD is often combined with other manual therapies including compression bandaging, exercise regimens, skin care techniques, pressure gradient garments, and pneumatic compression devices [ 1520 ].
Complex decongestive therapy (CDT) is a com­bined approach to lymphedema therapy that has been standardized by multiple international lym­phatic treatment organizations and specialized lymphedema treatment programs [ 10 , 1416 ]. The treatment regimen is composed of two phases: intensive reduction therapy followed by mainte­nance therapy (Table 23.3 ). This treatment regi- men utilizes MLD, compression wrapping, exercise therapy, and skin care. This highly suc­cessful treatment regimen has become the standard of care for lymphedema management [ 10 , 1416 ]. Signifi cant improvement and reduction of swelling is often readily apparent after treatment (Fig. 23.4 ).
Compression wrapping in various forms has been a long-standing treatment of both venous and lymphatic edema [ 10 , 1720 ]. Lymphatic wrapping techniques are complex and utilize low­stretch bandages instead of the more traditional high-stretch elastic bandages. High-stretch wrap­ping produces high pressures at rest that decrease with limb muscle contraction and movement. This
Increasing
compression
Fig. 23.6 Graduated compression stockings. Graduated
compression stockings have the highest pressure at the ankle level. The pressure decreases up the leg where the pressure is the lowest at the highest level. The ideal com­pression for lymphedema treatment is 30–40 mmHg
decreases the ability of the wrap to raise the tissue pressure during exercise, reducing the hydrostatic pressure gradient and resulting in a reduction in stimulation of lymphatic fl ow [ 10 , 1720 ].
In contrast, low-stretch wrapping provides resistance during muscle pump action that results in an increase in pressure gradient and stimulates increased fl uid fl ow [ 10 , 1720 ]. Patients with signifi cant obesity, pain problems, or advanced disease may not be able to comply with the com­plexities of wrapping. For these patients, static gradient compression devices are available.
The use of elastic compression garments is the mainstay of the maintenance portion of any lymphedema management program [ 10 , 1721 ]. Compliance with daily use of compression stock­ings or sleeves is critical for maintenance of limb size and volume. Compression garments should have graduated compression where pressure is highest distally and decreases proximally where the pressure is lowest at the highest level (Fig. 23.6 ). For an upper extremity graduated compression sleeve, pressure is highest at the hand/wrist and is lowest at the shoulder. For a lower extremity graduated compression stocking, pressure is highest at the ankle and is lowest at the
23 Lymphedema
https://t.me/med1917
Fig. 23.7 The Flexitouch
system pneumatic compres­sion device. This pneumatic compression device closely mimics manual lymphatic drainage with the use of multiple small compression chambers. Compression sleeves for the lower extremity ( top ) and upper extremities and trunk ( bottom ) are available
337
knee, thigh, or waist, depending on the length of the stocking. Recommended graduated compres­sion is 30–40 mmHg for the lower extremity [ 10 , 18 ]. Upper extremity lymphedema sleeves are available with a graduated compression of 20–30 mmHg, which is usually adequate [ 10 , 18 ].
In addition to providing graduated compres­sion, compression stockings and sleeves also assist with venous return, help preserve skin integrity, and protect the skin from trauma [ 10 ]. Currently, there are many manufacturers who produce graduated compression stockings and sleeves with different pressure strengths, differ­ent fabrics, and multiple color options. The abil­ity to independently don the compression garment is critical. Numerous devices are available to assist with stocking and sleeve donning.
For decades prior to the introduction of CDT, pneumatic compression pumps were the main­stay of lymphedema therapy. Since the mid­1990s, when CDT became more widely available, the use of pneumatic compression pump therapy has largely become an adjunct to CDT in both the reductive and maintenance phases [ 3 , 10 , 14 , 22 ]. The majority of pneumatic compression pumps perform sequential pumping of the affected lymphedematous limb from distal to proximal. These devices augment the benefi cial effects of the standard modalities of CDT. There is a new class of sequential pneumatic compression device, known as the Flexitouch system. This pneumatic compression device closely mimics MLD with the use of multiple small compression chambers (Fig. 23.7 ).
338
https://t.me/med1917
J. Laredo and B.B. Lee
23.8.3 Prevention of Infection
Prevention of acute episodes of cellulitis or lym­phangitis is critical because they cause severe deterioration in swelling and result in further injury to the lymphatic system [ 12 , 21 , 22 ]. Care of the skin, good hygiene, control of skin diseases such as tinea pedis, and careful antiseptic dressing application after minor wounds are all important. Antibiotics must be administered promptly when an acute infl ammatory episode occurs. There are no defi nitive studies addressing antibiotic prophy­laxis for patients at risk for lymphedema, but evidence has shown the relationship between chronic fungal infection and the development of cellulitis, which is known to increase the potential for lymphatic failure [ 12 , 22 ].
23.8.4 Pharmacologic Treatment
Diuretics are of little benefi t in patients with lymphedema because the pharmacologic effects only limit capillary fi ltration [ 2 , 3 ]. Improvement in lymphedema patients who are taking diuretics suggests that the predominant cause of edema is not lymphatic and is likely due to another undiag­nosed etiology. In cases where increased hydro­static pressure is also elevated, such as the postphlebitic syndrome with secondary hyper­tension, low-dose thiazide-induced diuresis may play a benefi cial complementary role to compres­sion therapy [ 12 ].
Coumarin, a benzopyrone medication, has been reported to be of benefi t to patients with lymphedema [ 23 ]. However, the poor study design of most of the coumarin trials limits inter­pretability. The therapeutic benefi t, if present, has been theoretically ascribed to its effects on cuta­neous macrophages and, thereby, on local prote­olysis. The medication also stimulates other cellular elements of the immune system and may promote protein reabsorption. Despite some encouraging early trials, coumarin must still be considered experimental [ 2325 ]. In addition, its associated risk of hepatotoxicity makes this med­ication an even much less attractive treatment option [ 3 , 23 ].
23.8.5 Surgical Therapy
In situations where CDT fails to improve the size and weight of a lymphedematous limb that is so large, it inhibits its use and interferes with mobil­ity and function, and surgery may be of value. Surgery is aimed at either removing excessive tissue (excisional procedures) or bypassing local lymphatic defects (lymphatic reconstruction pro­cedures) [ 4 , 26 ]. CDT is still required after surgi- cal excision and reconstruction.
Excisional procedures usually involve staged removal of the lymphedematous subcutaneous tissue of the leg [ 2629 ]. The most radical exci- sional operation, the Charles procedure, involves total skin and subcutaneous tissue excision of the lower extremity from the tibial tuberosity to the malleoli, followed by skin grafting. The main complications associated with this procedure and other excisional procedures are infection and necrosis of the skin graft [ 26 ].
Chronic lymphedematous tissue transforms with time into adipose tissue, which cannot be reduced by massage or compression treatment. Liposuction aimed at removing this adipose tis­sue has been reported to be benefi cial in treating lymphedematous limbs [ 28 , 29 ]. This procedure is not routinely performed for treatment of lymphedema.
Developments in microvascular techniques have allowed surgical attempts at direct lymphatic reconstructions, performance of lymphatic­venous anastomoses, or lymphatic grafting [ 26 , 30 , 31 ]. These reconstructions are usually indi- cated in only a small subset of patients who have proximal obstruction with preserved lymphatic vessels distally.
The best outcomes are seen in patients with secondary lymphedema, with well-defi ned trauma to the lymphatics, seen on lymphatic imaging, who underwent lymphatic to venous anastomoses [ 30 , 31 ].
Lymphatic bypass procedures are only per­formed in a few selected cases and in only a few specialized medical centers. This is refl ected in the literature by small patient numbers in most series reported [ 26 ]. Results are variable, and lymphatic bypass procedures are generally not
23 Lymphedema
https://t.me/med1917
339
routinely performed except at these few special­ized medical centers.
References
1. Dellinger MT, Bernas MJ, Witte MH. Lymphatic biol­ogy and pathobiology. In: Dieter RS, Dieter Jr RA, Dieter RA, editors. Venous and lymphatic diseases. New York: McGraw Hill; 2011. p. 17–36.
2. Thanaporn PK, Rockson SG. Disease of the lym­phatic vasculature. In: Dieter RS, Dieter Jr RA, Dieter RA, editors. Venous and lymphatic diseases. New York: McGraw Hill; 2011. p. 569–94.
3. Rockson SG. Diagnosis and management of lym­phatic vascular disease. J Am Coll Cardiol. 2008; 52(10):799–806.
4. Tiwari A, Cheng KS, Button M, Myint F, Hamilton G. Differential diagnosis, investigation, and current treatment of lower limb lymphedema. Arch Surg. 2003;138(2):152–61.
5. Ely JW, Osheroff JA, Chambliss ML, Ebell MH. Approach to leg edema of unclear etiology. J Am Board Fam Med. 2006;19(2):148–60.
6. Alitalo K, Tammela T, Petrova TV. Lymphangiogenesis in development and human disease. Nature. 2005; 438:946–53.
7. Rooke TW, Felty C. Lymphedema: pathophysiology, classifi cation, and clinical evaluation. In: Gloviczki P, editor. Handbook of venous disorders. 3rd ed. London: Hodder Arnold; 2009. p. 629–34.
8. Kerchner K, Fleischer A, Yosipovitch G. Lower extremity lymphedema update: pathophysiology, diagnosis, and treatment guidelines. J Am Acad Dermatol. 2008;59(2):324–31.
9. International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. 2009 Concensus Document of the International Society of Lymphology. Lymphology. 2009;42(2):51–60.
10. Gamble GL, Cheville A, Strick D. Lymphedema: medical and physical therapy. In: Gloviczki P, editor. Handbook of venous disorders. 3rd ed. London: Hodder Arnold; 2009. p. 649–57.
11. Lee B, Andrade M, Bergan J, Boccardo F, Campisi C, Damstra R, et al. Diagnosis and treatment of pri­mary lymphedema. Consensus document of the International Union of Phlebology (IUP)-2009. Int Angiol. 2010;29(5):454–70.
12. Mortimer PS. ABC of arterial and venous disease swollen lower limb – 2: Lymphoedema. BMJ. 2000; 320:1527–9.
13. Dean SM, Zirwas MJ, Horst AV. Elephantiasis nostras verrucosa: an institutional analysis of 21 cases. J Am Acad Dermatol. 2011;64(6):1104–10.
14. Cheville AL, McGarvey CL, Petrek JA, Russo SA, Taylor ME, Thiadens SR. Lymphedema management. Semin Radiat Oncol. 2003;13(3):290–301.
15. Mayrovitz HN. The standard of care for lymphedema: current concepts and physiological considerations. Lymphat Res Biol. 2009;7(2):101–8.
16. Badger C, Preston N, Seers K, Mortimer P. Physical therapies for reducing and controlling lymphoedema of the limbs. Cochrane Database Syst Rev. 2004;4, CD003141.
17. Partsch H, Mosti G. Thigh compression. Phlebology. 2008;23(6):252–8.
18. Partsch H, Flour M, Smith PC, International Compression Club. Indications for compression ther­apy in venous and lymphatic disease consensus based on experimental data and scientifi c evidence. Under the auspices of the IUP. Int Angiol. 2008;27(3): 193–219.
19. Pappas CJ, O’Donnell Jr TF. Long-term results of compression treatment for lymphedema. J Vasc Surg. 1992;16(4):555–62.
20. Damstra RJ, Brouwer ER, Partsch H. Controlled, comparative study of relation between volume changes and interface pressure under short-stretch bandages in leg lymphedema patients. Dermatol Surg. 2008;34(6):773–8.
21. Mortimer PS. Therapy approaches for lymphedema. Angiology. 1997;48(1):87–91.
22. Keeley VL. Lymphoedema and cellulitis: chicken or egg? Br J Dermatol. 2008;158(6):1175–6.
23. Badger C, Preston N, Seers K, Mortimer P. Benzo­pyrones for reducing and controlling lymphoedema of the limbs. Cochrane Database Syst Rev. 2004;2, CD003140.
24. Casley-Smith JR. Benzo-pyrones in the treatment of lymphoedema. Int Angiol. 1999;18(1):31–41.
25. Loprinzi CL, Kugler JW, Sloan JA, Rooke TW, Quella SK, Novotny P, et al. Lack of effect of coumarin in women with lymphedema after treatment for breast cancer. N Engl J Med. 1999;340(5):346–50.
26. Gloviczki P. Principles of surgical treatment of chronic lymphedema. In: Gloviczki P, editor. Handbook of venous disorders. 3rd ed. London: Hodder Arnold; 2009. p. 658–64.
27. Miller TA, Wyatt LE, Rudkin GH. Staged skin and subcutaneous excision for lymphedema: a favorable report of long-term results. Plast Reconstr Surg. 1998;102(5):1486–98.
28. Brorson H. From lymph to fat: complete reduction of lymphoedema. Phlebology. 2010;25 Suppl 1:52–63.
29. Brorson H, Ohlin K, Olsson G, Svensson B, Svensson H. Controlled compression and liposuction treatment for lower extremity lymphedema. Lymphology. 2008;41(2):52–63.
30. Campisi C, Bellini C, Campisi C, Accogli S, Bonioli E, Boccardo F. Microsurgery for lymphedema: clini­cal research and long-term results. Microsurgery. 2010;30(4):256–60.
31. Campisi C, Eretta C, Pertile D, Da Rin E, Campisi C, Macciò A, et al. Microsurgery for treatment of periph­eral lymphedema: long-term outcome and future perspectives. Microsurgery. 2007;27(4):333–8.
Venous Leg Ulcers
https://t.me/med1917
Robert B. McLafferty
2 4
Contents
24.1 Introduction ................................................ 341
24.2 Basic Principles .......................................... 342
24.2.1 History and Physical Examination ............... 342
24.2.2 Laboratory Assessment ................................ 343
24.2.3 Microbial Culture Evaluation ...................... 343
24.2.4 Skin/Ulcer Biopsy ........................................ 344
24.2.5 Wound Assessment ...................................... 344
24.2.6 Noninvasive Vascular Testing ...................... 344
24.2.7 X-Ray Evaluation......................................... 344
24.3 Venous Ulcers ............................................. 345
24.3.1 Epidemiology ............................................... 345
24.3.2 Pathophysiology ........................................... 345
24.3.3 History and Physical Examination ............... 345
24.3.4 Management................................................. 346
24.4 Leg Ulcer Differential Diagnosis............... 349
24.4.1 Arterial Ulcers .............................................. 349
24.4.2 Diabetic Ulcers ............................................ 349
24.4.3 Pressure Ulcers ............................................ 350
24.4.4 Infectious Ulcers .......................................... 350
24.4.5 Vasculitic Ulcers .......................................... 351
24.4.6 Pyoderma Gangrenosum .............................. 351
24.5 Summary..................................................... 351
References ................................................................. 352
Abstract
Venous leg ulcers are the most common form of leg ulcer. While there are many rare causes of ulcerations that can occur from knee to the toes, the overview provided herein gives the practitioner guidance on how to evaluate a patient presenting with a leg ulcer and care for and heal the venous ulcer and informa­tion about other more common types of ulcers that are in the differential diagnosis. Fortunately, history and physical examina­tion can help determine, with some confi r­matory tests, the type of ulcer. Nevertheless, the essentials of wound healing remain the same for the large majority of ulcers on the lower extremities. Healing will hasten if treatment of all leg ulcers includes assuring adequate perfusion; removing nonviable tis­sue; reducing infl ammation and eliminating infection, relieving edema; optimizing tissue growth; off-loading or providing pressure relief; controlling pain; and treating host sys­temic disease or conditions such as diabetes and nutrition.
R. B. McLafferty , MD, FACS, RVT Division of Vascular Surgery, Department of Surgery , Southern Illinois University, School of Medicine , Springfi eld , IL , USA e-mail: robert.mclafferty@va.gov
E. Mowatt-Larssen et al. (eds.), Phlebology, Vein Surgery and Ultrasonography, DOI 10.1007/978-3-319-01812-6_24, © Springer International Publishing Switzerland 2014
24.1 Introduction
Chronic ulceration of the lower leg and foot con­tinues to be one of the more formidable clinical problems in medicine. Conditions leading to ulceration of this susceptible region of the body frequently cause pain, disability, social stigma, and considerable costs. Burden on family
341
342
https://t.me/med1917
R.B. McLafferty
members, caretakers, and medical facilities as well as the economic strain from inability to work can be high, further complicating the path­way to healing. A staggering 1 % of the popula­tion will suffer from chronic ulceration of the leg during some time over a lifetime [ 1 , 2 ]. The prevalence of leg ulcerations increases with age and ranges from 3 to 5 % in the adult population over the age of 65 years [ 14 ]. In one study from the UK, the prevalence of venous ulcers alone in individuals over the age of 65 was estimated to be 1–2 % [ 5 ].
Although there are varying defi nitions of the term ulcer, the two prerequisites include full thickness obliteration of the epidermis and der­mis with no sources of epithelialization in the center of the ulcer combined with the tendency of slow healing. Generally, as compared to an acute wound, a slow-healing ulcer is defi ned as being present for more than 4 weeks. Reasons for chronic ulcers are not necessarily related to depth and size but often associated with an underlying disease manifestation (systemic, local, or both) that requires specialized treatment in order to induce healing.
Dividing the causes of ulcers into common and rare etiologies helps in the construction of an accurate differential diagnosis. The most common causes of leg ulcers are chronic venous disease (45–90 %), diabetes mellitus (15–25 %), arterial ischemia (10–20 %), or a combination of two or more of these etiologies (10–15 %) [ 69 ]. Less common causes of ulcers, but not necessarily rare, include infections, decubitus (pressure), and vasculitis. This chapter will pri­marily focus on the diagnosis and care for venous leg ulcers and also briefl y outline evalu­ation and treatment options of other causes of leg ulcers in the differential diagnosis. The importance of correct diagnosis cannot be over emphasized as diagnostic tests and treatments can vary dramatically. Alternatively stated, incorrect diagnosis can lead to incorrect treat­ment and hence result in further harm to the patient with a leg ulcer.
24.2 Basic Principles
24.2.1 History and Physical Examination
When performing a fi rst-time evaluation on a new patient with a chronic leg ulcer, several basic principles should be followed in addition to a complete history and physical examination. The patient’s story of how the ulceration began is important and may give rise to clues as to the type of ulcer. Did the ulcer occur spontaneously from seemingly normal-appearing skin or were there preceding symptoms or signs such as pain, tenderness, itching, swelling, skin discoloration, infl ammatory changes, or blisters? Other impor­tant aspects of the ulcer include location, size, duration, and symptoms. Do the symptoms vary with time of day or position?
Further clues in the history regarding the patient’s overall medical condition include whether or not the patient has had deep venous thrombosis or pulmonary embolism; whether the patient has diabetes mellitus; and whether the patient has risk factors for atherosclerotic disease such as smoking, hypertension, hyperlipidemia, or chronic renal insuffi ciency. Past history of other events related to atherosclerosis such as stroke, coronary artery disease, or claudication should be elicited. Infl ammatory conditions such as rheumatoid arthritis, lupus erythematosus, or infl ammatory bowel disease are also important. Other pertinent information include whether the patient has had fever or rigors, recent trauma or surgery, a change in types of shoes being worn, or a history of whether there are any sensory defi ­cits, particularly in the forefoot.
The physical exam from below the knees to the toes requires close methodical inspection and palpation. Vitally important areas to be assessed include the skin on the posterior heel and ankle as well as the web spaces between the toes. Nails deserve close scrutiny and should be described in detail. Bony deformities such as partial foot amputation, bunion, hammertoes, metatarsal head